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ダウンロード数 : ?
ID 25669
著者
ノダ, サトシ Department of Radiology, The University of Tokushima School of Medicine
岸, 和弘 Division of Molecular Genetics, Institute for Enzyme Research, The University of Tokushima
湯浅, 智之 Division of Molecular Genetics, Institute for Enzyme Research, The University of Tokushima 徳島大学 教育研究者総覧 KAKEN研究者をさがす
ハヤシ, ヒデキ Division of Molecular Genetics, Institute for Enzyme Research, The University of Tokushima
オオニシ, テツオ Division of Molecular Genetics, Institute for Enzyme Research, The University of Tokushima
ミヤタ, イクコ Division of Molecular Genetics, Institute for Enzyme Research, The University of Tokushima
西谷, 弘 Department of Radiology, The University of Tokushima School of Medicine 徳島大学 教育研究者総覧 KAKEN研究者をさがす
蛯名, 洋介 Division of Molecular Genetics, Institute for Enzyme Research, The University of Tokushima 徳島大学 教育研究者総覧 KAKEN研究者をさがす
キーワード
AKT
p70S6 kinase
GSK3β
GLUT4
資料タイプ
学術雑誌論文
抄録
We have developed a simple, direct and sensitive method to detect GLUT4 on the cell surface. Using this system, we found that PI3-kinase plays a key role in the signaling pathway of insulin-stimulated GLUT4 translocation. One of the down stream effectors of PI3-kinase is serine-threonine kinase Akt (protein kinase B, RAK-PK), but the involvement of Akt in insulin-stimulated GLUT4 translocation is controversial. To investigate whether Akt1 regulates insulin-stimulated GLUT4 translocation and glucose uptake in L6 myotubes, we established L6 myotubes stably expressing c-myc epitope-tagged GLUT4 (GLUT4myc) and mouse wild type (WT) Akt1. We found that overexpression of WT Akt1 promoted insulin-stimulated p70S6 kinase (p70S6K) activity and increased the basal activity of GSK3β, but did not promote insulin-stimulated GLUT4translocation or glucose uptake. These data supported the result that Akt is not a main signaling molecule to transmit the signal of insulin-stimulated GLUT4 translocation or glucose uptake from insulin-activated PI3-kinase.
掲載誌名
The journal of medical investigation : JMI
ISSN
13431420
cat書誌ID
AA11166929
47
1-2
開始ページ
47
終了ページ
55
並び順
47
発行日
2000
備考
EDB ID
フルテキストファイル
言語
eng
部局
医学系
先端酵素学研究所